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, Dans cette étude, il est montré que l'absence d'Alix (ALG-2 interacting protein-X) entraîne des modifications morphologiques et fonctionnelles des synapses qui pourraient être la conséquence d'un recyclage défectueux des VS. Nous avons récemment montré que Alix et l'un de ses partenaires, l'endophiline-A, sont essentiels pour l'endocytose indépendante de la clathrine dans les fibroblastes, ce qui nous amène à penser que Alix pourrait jouer le même rôle dans le bouton pré-synaptique. Au cours de ce travail, j'ai montré que Alix se concentre au niveau des boutons pré-synaptiques après une stimulation à haute fréquence des neurones. En utilisant des formes mutantes d'Alix, j'ai montré que le recrutement d'Alix à la membrane pré-synaptique était dépendant de son interaction avec ALG-2 (protéine de liaison au calcium). De même la relocalisation de l'endophiline-A à la synapse est dépendante de son interaction avec Alix. Par ailleurs, l'absence d'Alix dans les neurones conduit à une altération de l'ADBE, qui peut être restaurée par l'expression d'Alix, mais pas avec ses mutants incapables d, Résumé La neurotransmission nécessite la fusion de vésicules synaptiques (VS) avec la membrane pré-synaptique pour libérer les neurotransmetteurs qui vont activer les récepteurs du neurone postsynaptique. Le nombre de VS dans le bouton pré-synaptique est limité, ce qui nécessite des mécanismes efficaces pour régénérer ces vésicules